What are the learning objectives of your session?

What is the importance of the topic?

What are the recommended readings ahead of your session?

The FENS Forum 2020 Plenary and Special Lecture speakers addresses these questions and more for you.

Find out what they had to share with the community and stay tuned for new additions!

Andreas Meyer-Lindenberg

Neural mechanisms of environmental risk for psychiatric disorders.

Please introduce the learning objectives of your lecture.

The lecture is about Neural mechanisms of environmental risk for psychiatric disorders. Risk factors such as city life, migration or social status are well known but how they influence brain function and structure to make people liable to mental illness is just coming into focus, as this lecture will explain.

Why is this topic important?

Mental disorders cost more than 500 billion euros in the EU annually and are the main source of disease burden in the young and working population. The appropriate medical response to a problem of this size is prevention, for which one needs to understand how components of the environment influence the brain. As urbanization, migration and climate change subject humans to ecological changes of unprecedented rapidity we hope that this work helps in identifying resilience factors and mitigate risk exposures that further mental health and well-being.

What are the recommended readings ahead of your lecture?

Tost, H., F. A. Champagne and A. Meyer-Lindenberg (2015). “Environmental influence in the brain, human welfare and mental health.” Nat Neurosci 18(10): 1421-1431.

Tost, H., M. Reichert, U. Braun, I. Reinhard, R. Peters, S. Lautenbach, A. Hoell, E. Schwarz, U. Ebner-Priemer, A. Zipf and A. Meyer-Lindenberg (2019). “Neural correlates of individual differences in affective benefit of real-life urban green space exposure.” Nat Neurosci.

van den Bosch, M. and A. Meyer-Lindenberg (2019). “Environmental Exposures and Depression: Biological Mechanisms and Epidemiological Evidence.” Annu Rev Public Health.

Angela Roberts

Prefrontal circuits related to anxiety and anhedonia

Please introduce the learning objectives of your lecture

There are multiple, interacting, cognitively specific circuits within primate prefrontal cortex contributing to emotion regulation. The surprisingly distinct developmental trajectories of these circuits highlight the possibility that stress, a key risk factor for affective disorder onset, may induce distinct patterns of cognitive and emotional deficits at different developmental stages.

Why is this topic important?

Anxiety and anhedonia are core symptoms of a number of neurodevelopmental, psychiatric and neurodegenerative disorders. The mixed aetiology of these symptoms however underlies the high variability in overall treatment success. A detailed understanding therefore, of the prefrontal circuits that, if dysregulated, can lead to an anxiety-like and anhedonia-like phenotype is an important step along the pathway to the development of novel treatment strategies and individualised therapy.

What are the recommended readings ahead of your lecture?

Roberts, A.C. (2020) Prefrontal Regulation of Threat-Elicited Behaviors: A Pathway to Translation. Annual Review of Psychology. epub ahead of print

https://www.annualreviews.org/doi/pdf/10.1146/annurev-psych-010419-050905

Alexander, A., Clarke, H.F., Roberts, A.C. A Focus on the functions of area 25. (2019) Brain Sciences 9:129.

https://www.ncbi.nlm.nih.gov/pubmed/31163643

Sawiak S.J., Shiba Y., Oikonomidis L., Windle C.P., Santangelo A.M., Grydeland H., Cockcroft G., Bullmore E.T, Roberts A.C.  Trajectories and milestones of cortical and subcortical development of the marmoset brain from infancy to adulthood.  (2018) Cerebral Cortex 28:4440-4453.

https://www.ncbi.nlm.nih.gov/pubmed/30307494

Carla Shatz

Synapses lost and found: developmental critical periods and Alzheimer’s Disease. 

Please introduce the learning objectives of your lecture.

In this lecture we will consider mechanisms of activity-dependent synapse pruning during a normal developmental critical period and how this knowledge of a fundamental developmental process has led to the discovery of an innate immune receptor for soluble oligomers of beta amyloid expressed by cortical neurons, and a new way of thinking about therapeutic approaches to treating Alzheimer’s disease.

Why is this topic important?

There is enormous interest in mechanisms controlling pruning and removal of synapses in both health and disease. Given recent disappointing failures of clinical trials for Alzheimer’s disease, new approaches are urgently needed.

What are the recommended readings ahead of your lecture?

Activity-dependent modulation of hippocampal synaptic plasticity via PirB and endocannabinoids. Djurisic M, Brott BK, Saw NL, Shamloo M, Shatz CJ. Mol Psychiatry. 2019 Aug;24(8):1206-1219

Neuron-Glia Signaling in Synapse Elimination. Wilton DK, Dissing-Olesen L, Stevens B. Annu Rev Neurosci. 2019 Jul 8;42:107-127.

Synapse elimination and learning rules co-regulated by MHC class I H2-Db. Lee H, Brott BK, Kirkby LA, Adelson JD, Cheng S, Feller MB, Datwani A, Shatz CJ. Nature. 2014 May 8;509(7499):195-200

Human LilrB2 is a β-amyloid receptor and its murine homolog PirB regulates synaptic plasticity in an Alzheimer’s model. Kim T, Vidal GS, Djurisic M, William CM, Birnbaum ME, Garcia KC, Hyman BT, Shatz CJ. Science. 2013 Sep 20;341(6152):1399-404

MHC class I: an unexpected role in neuronal plasticity. Shatz CJ. Neuron. 2009 Oct 15;64(1):40-5

Mechanisms underlying development of visual maps and receptive fields. Huberman AD, Feller MB, Chapman B. Annu Rev Neurosci. 2008;31:479-509.

Hugues Chabriat

CADASIL: a clinical model of ischemic small vessel disease.

Please introduce the learning objectives of your lecture.

A large number of magnetic resonance imaging markers are detected with aging or in stroke patients. Their exact pathophysiology remains largely undetermined. CADASIL represents a unique model for exploring the origin, clinical consequences and development of these lesions. The main lessons of research in this area will be presented.

Why is this topic important?

Understanding small vessel disease imaging markers is essential to better understand their clinical impact, their development, and their potential usefulness for developing prevention and future therapeutic trials in cerebral small vessel diseases.

What are the recommended readings ahead of your lecture?

CADASIL. Chabriat H, Joutel A, Dichgans M, Tournier-Lasserve E, Bousser MG. Lancet Neurol. 2009 Jul;8(7):643-53.

Brain atrophy is related to lacunar lesions and tissue microstructural changes in CADASIL. Jouvent E, Viswanathan A, Mangin JF, O’Sullivan M, Guichard JP, Gschwendtner A, Cumurciuc R, Buffon F, Peters N, Pachaï C, Bousser MG, Dichgans M, Chabriat H. Stroke. 2007 Jun;38(6):1786-90.

Impact of MRI markers in subcortical vascular dementia: a multi-modal analysis in CADASIL.Viswanathan A, Godin O, Jouvent E, O’Sullivan M, Gschwendtner A, Peters N, Duering M, Guichard JP, Holtmannspötter M, Dufouil C, Pachai C, Bousser MG, Dichgans M, Chabriat H. Neurobiol Aging. 2010 Sep;31(9):1629-36.

Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration. Wardlaw JM, Smith EE, Biessels GJ, Cordonnier C, Fazekas F, Frayne R, Lindley RI, O’Brien JT, Barkhof F, Benavente OR, Black SE, Brayne C, Breteler M, Chabriat H, Decarli C, de Leeuw FE, Doubal F, Duering M, Fox NC, Greenberg S, Hachinski V, Kilimann I, Mok V, Oostenbrugge Rv, Pantoni L, Speck O, Stephan BC, Teipel S, Viswanathan A, Werring D, Chen C, Smith C, van Buchem M, Norrving B, Gorelick PB, Dichgans M. Lancet Neurol. 2013 Aug;12(8):822-38.

Different Types of White Matter Hyperintensities in CADASIL. Duchesnay E, Hadj Selem F, De Guio F, Dubois M, Mangin JF, Duering M, Ropele S, Schmidt R, Dichgans M, Chabriat H, Jouvent E. Front Neurol. 2018 Jul 10;9:526

Pathogenesis of white matter changes in cerebral small vessel diseases: beyond vessel-intrinsic mechanisms. Joutel A, Chabriat H. Clin Sci (Lond). 2017 Apr 25;131(8):635-651.

Laurence Hunt

Prefrontal circuits for decision making.

Please introduce the learning objectives of your lecture.

My lecture will discuss the contribution of different subregions of prefrontal cortex to reward-guided decision making. By recording populations of neurons from macaque orbitofronal, anterior cingulate and dorsolateral prefrontal cortex during an attention-guided decision making task, we have isolated the unique computations performed by each subregion as a decision is formed.

Why is this topic important?

The prefrontal cortex is one of the regions that has expanded most during primate and human evolution. It underlies our most sophisticated cognitive abilities. Understanding the neural basis of these abilities may be particularly relevant to the current ‘hot topic’ of artificial intelligence, which explores how we can train artificial agents to perform sophisticated cognitive tasks that likely depend upon prefrontal cortex in primates.

What are the recommended readings ahead of your lecture?

Triple Dissociation of Attention and Decision Computations across Prefrontal Cortex, Hunt et al. Nature Neuroscience 2018 (open access version available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6331040/)

A distributed, hierarchical and recurrent framework for reward-based choice, Hunt and Hayden, Nature Reviews Neuroscience 2017 (open access version available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5621622/).

Why is FENS important for European and global neuroscience?

Neuroscience is a highly interdisciplinary field. FENS is important in that it brings together neuroscientists working in a very wide range of different backgrounds and on different topics. It provides a unique opportunity to gain an overview of current neuroscience research, ranging from cellular and molecular studies all the way up to studying systems and cognitive neuroscience.

What have been key breakthroughs since FENS 2018?

A major breakthrough has been the release of new recording technologies to record large numbers of single units simultaneously (NeuroPixels). I look forward to seeing the first wave of results with these electrodes presented at FENS 2020.

Sheena Josselyn

The amygdala and memory: recalling the past, imaging the future.

Please introduce the learning objectives of your lecture.

Understanding how the brain acquires, stores and uses information is a fundamental goal of neuroscience. As several human disorders (from autism spectrum disorder to Alzheimer’s disease) may stem from disrupted information processing, this basic knowledge is not only critical for understanding normal brain function, but also for the development of new treatment strategies.

Recently, with the introduction of new technologies allowing researchers to image and manipulate the brain of rodents at the level of individual neuron has reinvigorated memory research.

Memory, the ability to use the past in service of the present or future, is a hugely important topic. Memory is central to our everyday lives and defines who we are. Without it, we are condemned to an eternal present.

Tara Spires-Jones

Neuron-Glia interactions in synapse degeneration in Alzheimer’s Disease.

Please introduce the learning objectives of your lecture.

In my lecture, attendees will learn about synaptic pathology in Alzheimer’s disease and our progress on understanding mechanisms underlying this pathology, and how we might prevent or reverse synaptic damage in future.

Why is this topic important?

Dementia affects more than 50 million people worldwide, and we currently do not have any treatments that can modify the course of the disease.  Synapse degeneration is the strongest pathological correlate of cognitive decline in Alzheimer’s disease, the most common cause of dementia. Further, synapses are very adaptable and have the potential to contribute to cognitive recovery if we can prevent or reverse synaptic damage.

What are the recommended readings ahead of your lecture?

Henstridge, C. M., Hyman, B. T. and Spires-Jones, T. L.* (2019). Beyond the neuron-cellular interactions early in Alzheimer disease pathogenesis. Nature Reviews Neuroscience, 20(2), 94-108. doi:10.1038/s41583-018-0113-1

Pickett, E. K., Rose, J., McCrory, C., McKenzie, C. A., King, D., Smith, C., Gillingwater, T. H., Henstridge, C. M. & Spires-Jones, T. L. Region-specific depletion of synaptic mitochondria in the brains of patients with Alzheimer’s disease. Acta Neuropathol, doi:10.1007/s00401-018-1903-2 (2018).

Pickett, E. K., Henstridge, C. M., Allison, E., Pitstick, R., Pooler, A., Wegmann, S., Carlson, G., Hyman, B. T. & Spires-Jones, T. L. Spread of tau down neural circuits precedes synapse and neuronal loss in the rTgTauEC mouse model of early Alzheimer’s disease. Synapse 71, doi:10.1002/syn.21965 (2017).

Kay, K. R., Smith, C., Wright, A. K., Serrano-Pozo, A., Pooler, A. M., Koffie, R., Bastin, M. E., Bak, T. H., Abrahams, S., Kopeikina, K. J., McGuone, D., Frosch, M. P., Gillingwater, T. H., Hyman, B. T. & Spires-Jones, T. L. Studying synapses in human brain with array tomography and electron microscopy. Nat Protoc 8, 1366-1380, doi:10.1038/nprot.2013.078 (2013).

Koffie, R. M., Hashimoto, T., Tai, H. C., Kay, K. R., Serrano-Pozo, A., Joyner, D., Hou, S., Kopeikina, K. J., Frosch, M. P., Lee, V. M., Holtzman, D. M., Hyman, B. T. & Spires-Jones, T. L. Apolipoprotein E4 effects in Alzheimer’s disease are mediated by synaptotoxic oligomeric amyloid-beta. Brain : a journal of neurology 135, 2155-2168, doi:10.1093/brain/aws127 (2012).

Why is FENS important for European and global neuroscience?

FENS provides key support for European and Global neuroscience through advocacy for funding, raising public awareness of the importance of neuroscience, providing networking and meeting opportunities, and advertising jobs!